BACKGROUND: β-Microseminoprotein (MSMB) is an abundant protein in seminal plasma. Most of it is present as a free protein but a small part is bound to cysteine-rich secretory protein 3 (CRISP3) as a non-covalent complex. Even though their physiological function is unknown, both MSMB and CRISP3 have been ascribed roles in prostate carcinogenesis. Thus, several recent experimental studies indicate a tumor-suppressor role for MSMB. The present study was undertaken in order to evaluate, for the first time, the expression of MSMB and CRISP3 in ovaries and in ovarian tumors and to determine if their expression might indicate a role in ovarian tumor development. MATERIALS AND METHODS: Biopsies from prospectively collected samples from ovaries and benign, borderline and invasive ovarian tumors were analyzed for expression of MSMB and CRISP3 by immunohistochemistry. In patients with ovarian cancer the expression was compared to survival. RESULTS: Both MSMB and CRISP3 were strongly stained in ovarian epithelial cells and weakly stained in the stroma. In ovarian blood vessels, CRISP3 exhibited strong to medium staining, while MSMB was only weakly expressed. In benign and borderline tumors the staining pattern was similar to the one observed in the ovaries. In invasive neoplasms, the expression of MSMB in the tumor cells was significantly reduced. In univariate analysis, decreased expression of MSMB correlated to reduced survival. No correlation was found with stage, the strongest prognostic indicator for ovarian cancer, which supports an independent role of MSMB in ovarian carcinogenesis. For CRISP3, a staining pattern comparable to that for MSMB was observed in all groups, except the fact that decreased expression was not observed in invasive tumor cells. CONCLUSION: MSMB and CRISP3 were widely distributed in ovaries and in ovarian tumors; the expression of MSMB fits well with a tumor-suppressor function in ovarian carcinogenesis.
BACKGROUND: β-Microseminoprotein (MSMB) is an abundant protein in seminal plasma. Most of it is present as a free protein but a small part is bound to cysteine-rich secretory protein 3 (CRISP3) as a non-covalent complex. Even though their physiological function is unknown, both MSMB and CRISP3 have been ascribed roles in prostate carcinogenesis. Thus, several recent experimental studies indicate a tumor-suppressor role for MSMB. The present study was undertaken in order to evaluate, for the first time, the expression of MSMB and CRISP3 in ovaries and in ovarian tumors and to determine if their expression might indicate a role in ovarian tumor development. MATERIALS AND METHODS: Biopsies from prospectively collected samples from ovaries and benign, borderline and invasive ovarian tumors were analyzed for expression of MSMB and CRISP3 by immunohistochemistry. In patients with ovarian cancer the expression was compared to survival. RESULTS: Both MSMB and CRISP3 were strongly stained in ovarian epithelial cells and weakly stained in the stroma. In ovarian blood vessels, CRISP3 exhibited strong to medium staining, while MSMB was only weakly expressed. In benign and borderline tumors the staining pattern was similar to the one observed in the ovaries. In invasive neoplasms, the expression of MSMB in the tumor cells was significantly reduced. In univariate analysis, decreased expression of MSMB correlated to reduced survival. No correlation was found with stage, the strongest prognostic indicator for ovarian cancer, which supports an independent role of MSMB in ovarian carcinogenesis. For CRISP3, a staining pattern comparable to that for MSMB was observed in all groups, except the fact that decreased expression was not observed in invasive tumor cells. CONCLUSION:MSMB and CRISP3 were widely distributed in ovaries and in ovarian tumors; the expression of MSMB fits well with a tumor-suppressor function in ovarian carcinogenesis.
Authors: Stefan Enroth; Malin Berggrund; Maria Lycke; John Broberg; Martin Lundberg; Erika Assarsson; Matts Olovsson; Karin Stålberg; Karin Sundfeldt; Ulf Gyllensten Journal: Commun Biol Date: 2019-06-20